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Photodynamic therapy (PDT) has become a promising candidate for cancer theranostics; however, traditional photosensitizers (PSs) usually exhibit weak fluorescence and poor reactive oxygen species (ROS) generation efficiency when aggregated. Recently, aggregation‐induced emission (AIE) luminogens have shown great potential in the development of novel PSs owing to their excellent aggregation‐induced ROS generation (AIG‐ROS) activity. However, there are still concerns that must be addressed. In this study, two near‐infrared (NIR) emitters (PI and PTI) are synthesized with AIG‐ROS characteristic. PTI exhibit a valuable redder emission with more effective intersystem crossing (ISC) process than PI. The two AIE‐active PSs show excellent lipid droplet (LD)‐specific targeting ability. The detailed therapeutic mechanism of PDT in LDs specificity is also investigated. The mechanism of oxidation of polyunsaturated fatty acids (PUFAs) in LDs to form toxic lipid peroxides (LPOs) and thereby causing cellular ferroptosis is confirmed first. Homologous targeting is also used to achieve tumor targeting via coating PSs with active cancer cell membranes. Biomimetic aggregates exhibit good targeting ability, and an improved PDT antitumor effect via AIG‐ROS activity. These findings offer a clear route to develop advanced PSs with good targeting specificity. A template has also been provided for studying the therapeutic mechanism of AIE‐active PSs. The process of photodynamic therapy in the lipid droplets becomes clear via cellular ferroptosis caused by singlet oxygen species oxidating polyunsaturated fatty acids to form toxic lipid peroxides, and the strategy of homologous anticancer targeting is employed to achieve precise tumor targeting, which exhibits better suppression and even elimination of tumor growth.

Nanozymes, nanomaterials with enzyme-like activities, are becoming powerful competitors and potential substitutes for natural enzymes because of their excellent performance. Nanozymes offer better structural stability over their respective natural enzymes. In consequence, nanozymes exhibit promising applications in different fields such as the biomedical sector (in vivo diagnostics/and therapeutics) and the environmental sector (detection and remediation of inorganic and organic pollutants). Prussian blue nanoparticles and their analogues are metal–organic frameworks (MOF) composed of alternating ferric and ferrous irons coordinated with cyanides. Such nanoparticles benefit from excellent biocompatibility and biosafety. Besides other important properties, such as a highly porous structure, Prussian blue nanoparticles show catalytic activities due to the iron atom that acts as metal sites for the catalysis. The different states of oxidation are responsible for the multicatalytic activities of such nanoparticles, namely peroxidase-like, catalase-like, and superoxide dismutase-like activities. Depending on the catalytic performance, these nanoparticles can generate or scavenge reactive oxygen species (ROS).

Reactive oxygen species (ROS) play an essential role in physiological and pathological processes. Studies on the regulation of ROS for disease treatments have caused wide concern, mainly involving the topics in ROS‐regulating therapy such as antioxidant therapy triggered by ROS scavengers and ROS‐induced toxic therapy mediated by ROS‐elevation agents. Benefiting from the remarkable advances of nanotechnology, a large number of nanomaterials with the ROS‐regulating ability are developed to seek new and effective ROS‐related nanotherapeutic modalities or nanomedicines. Although considerable achievements have been made in ROS‐based nanomedicines for disease treatments, some fundamental but key questions such as the rational design principle for ROS‐related nanomaterials are held in low regard. Here, the design principle can serve as the initial framework for scientists and technicians to design and optimize the ROS‐regulating nanomedicines, thereby minimizing the gap of nanomedicines for biomedical application during the design stage. Herein, an overview of the current progress of ROS‐associated nanomedicines in disease treatments is summarized. And then, by particularly addressing these known strategies in ROS‐associated therapy, several fundamental and key principles for the design of ROS‐associated nanomedicines are presented. Finally, future perspectives are also discussed in depth for the development of ROS‐associated nanomedicines. Reactive Oxygen Species (ROS)‐regulating nanomedicines for disease treatments mainly include ROS‐upregulating nanomedicines and ROS‐downregulating nanomedicines. Here, ROS‐upregulating nanomedicines can exert the toxic effect by employing nanoplatforms to enhance ROS generation in pathological sites for ROS‐induced toxic therapy, and ROS‐downregulating nanomedicines can scavenge excess ROS to maintain normal physiological process and avoid oxidative stress injuries for antioxidant therapy.

Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible. As the mitochondrial generation of ROS increases, they can deactivate components of the respiratory chain and enzymes of the Krebs cycle, and mitochondria release a high amount of ROS that damage cellular structures. More recently, the feature of the mitochondrial antioxidant system, which does not specifically deal with intramitochondrial ROS, was discovered. Indeed, the mitochondrial antioxidant system detoxifies exogenous ROS species at the expense of reducing the equivalents generated in mitochondria. Thus, mitochondria are also a sink of ROS. These observations highlight the importance of the mitochondrial antioxidant system, which should be considered in our understanding of ROS-regulated processes. These processes include cell signaling and the progression of metabolic and neurodegenerative disease.

Here, the intensity and ratio of superoxide anion (O 2 • ), hydrogen peroxide (H 2 O 2 ) and hydroxyl anion (OH •- ) formation along the in vitro shootlets of four pear ( Pyrus communis L.) rootstocks (i.e., Pyrodwarf, OH × F40, OH × F69 and OH × F333) were scrutinized under E. amylovora inoculation, over 144 hpi. Furthermore, following identifying the most tolerant and susceptible pear rootstocks (i.e., OH × F69 and OH × F40, respectively), the dynamic expression profiles of three ROS-scavenging enzymatic genes including superoxide dismutase ( SOD ), Catalase ( CAT ) and ascorbate peroxidase ( APX ) were elucidated in response to E. amylovora , over 96 hpi. The highest disease tolerance was observed in OH × F69, and OH × F333, Pyrodwarf and OH × F40 occupied the next descending positions, respectively. Furthermore, the O 2 •- generation rates were almost similar in all the pears studied, though the accumulation of H 2 O 2 and OH •- and intensities thereof were considerably distinctive and significantly followed up the levels of disease resistance. Comparing to the controls (0 hpi), in both susceptible and tolerant pear rootstocks, transcription activity of SOD , CAT , and APX genes were overall stimulated with relatively high abundance over 24, 48, 72 and 96 hpi, though some fluctuations were also recorded. Our ROS results, altogether, indicated that E. amylovora is capable enough to stimulate ROS formation in pear, though its progress is extremely dependent upon the susceptibility ratio of the plant. Lastly, the particular expression patterns and different response time of three genes designated that pear rootstocks differentially activates genes encoding antioxidant enzymes to mitigate the possible damage of ROS during E. amylovora invasion.

The objective of this study was to investigate molecular mechanisms underlying the ability of carnosic acid to attenuate an early increase in reactive oxygen species (ROS) levels during MDI-induced adipocyte differentiation. The levels of superoxide anion and ROS were determined using dihydroethidium (DHE) and 2′-7′-dichlorofluorescin diacetate (DCFH-DA), respectively. Both superoxide anion and ROS levels peaked on the second day of differentiation. They were suppressed by carnosic acid. Carnosic acid attenuates the translation of NADPH (nicotinamide adenine dinucleotide phosphate) oxidase 4 (Nox4), p47phox, and p22phox, and the phosphorylation of nuclear factor-kappa B (NF-κB) and NF-κB inhibitor (IkBa). The translocation of NF-κB into the nucleus was also decreased by carnosic acid. In addition, carnosic acid increased the translation of heme oxygenase-1 (HO-1), γ–glutamylcysteine synthetase (γ-GCSc), and glutathione S-transferase (GST) and both the translation and nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2). Taken together, these results indicate that carnosic acid could down-regulate ROS level in an early stage of MPI-induced adipocyte differentiation by attenuating ROS generation through suppression of NF-κB-mediated translation of Nox4 enzyme and increasing ROS neutralization through induction of Nrf2-mediated translation of phase II antioxidant enzymes such as HO-1, γ-GCS, and GST, leading to its anti-adipogenetic effect.

1,4-Naphthoquinones have antibacterial activity and are a promising new class of compound that can be used to treat bacterial infections. The goal was to improve effective antibacterial agents; therefore, we synthesized a new class of naphthoquinone hybrids, which contain phenylamino-phenylthio moieties as significant counterparts. Compound 4 was modified as a substituted aryl amide moiety, which enhanced the antibacterial activity of earlier compounds 3 and 4. In this study, five bacterial strains Staphylococcus aureus (S. aureus), Listeria monocytogenes (L. monocytogenes), Escherichia coli (E. coli), Pseudomonas aeruginosa (P. aeruginosa) and Klebsiella pneumoniae (K. pneumoniae) were used to evaluate the antibacterial potency of synthesized naphthoquinones using the minimal inhibitory concentration (MIC) method. Most of the studied naphthoquinones demonstrated major antibacterial activity with a MIC of 15.6 µg/mL–500 µg/mL. Selected compounds (5a, 5f and 5x) were studied for the mode of action, using intracellular ROS generation, determination of apoptosis by the Annexin V-FITC/PI assay, a bactericidal kinetic study and in silico molecular modelling. Additionally, the redox potentials of the specified compounds were confirmed by cyclic voltammetry (CV).

Zinc oxide nanoparticles (ZnONPs) have become the widely used metal oxide nanoparticles and drawn the interest of global researchers due to their biocompatibility, low toxicity, sustainability and cost-effective properties. Due to their unique optical and chemical properties, it emerges as a potential candidate in the fields of optical, electrical, food packaging and biomedical applications. Biological methods using green or natural routes are more environmentally friendly, simple and less use of hazardous techniques than chemical and/or physical methods in the long run. In addition, ZnONPs are less harmful and biodegradable while having the ability to greatly boost pharmacophore bioactivity. They play an important role in cell apoptosis because they enhance the generation of reactive oxygen species (ROS) and release zinc ions (Zn2+), causing cell death. Furthermore, these ZnONPs work well in conjunction with components that aid in wound healing and biosensing to track minute amounts of biomarkers connected to a variety of illnesses. Overall, the present review discusses the synthesis and most recent developments of ZnONPs from green sources including leaves, stems, bark, roots, fruits, flowers, bacteria, fungi, algae and protein, as well as put lights on their biomedical applications such as antimicrobial, antioxidant, antidiabetic, anticancer, anti-inflammatory, antiviral, wound healing, and drug delivery, and modes of action associated. Finally, the future perspectives of biosynthesized ZnONPs in research and biomedical applications are discussed.

Urethane dimethacrylate (UDMA) is a dimethacrylate-based resin monomer that can react with other related monomers and inorganic particles, causing hydrophobic polymerization through cross-linking upon light activation. UDMA polymers are commonly used for the reconstruction and reinforcement of teeth and bones. UDMA can become unbound and be released from light-cured polymer resins. Thus far, no evidence exists on the toxic effects of UDMA and its related working mechanisms for macrophages. Therefore, in the present study, we investigated the cytotoxicity, mode of cell death, DNA damage, caspase activities, mitochondrial dysfunction, and reactive oxygen species (ROS) generation in RAW264.7 macrophages treated with UDMA using the lactate dehydrogenase (LDH) assay kit, Annexin V-FITC and PI assays, micronucleus formation and comet assay, caspase fluorometric assay, JC-1 assay, and 2ʹ,7ʹ-dichlorofluorescin diacetate (DCFH-DA) assay, respectively. Our results show that UDMA induced cytotoxicity; apoptosis and necrosis; genotoxicity, which is also called DNA damage; increased caspase-3, -8, and -9 activities; mitochondrial dysfunction; and intracellular ROS generation in a concentration-dependent manner in RAW264.7 macrophages. Thus, based on the observed inhibited concentration parallel trends, we concluded that UDMA induces toxic effects in macrophages. Furthermore, UDMA-induced intracellular ROS generation, cytotoxicity, and DNA damage were reduced by N-acetyl-L-cysteine.

Here, we report a new synthetic protocol based on microwave-assisted synthesis (MAS) for the preparation of higher yields of zinc and copper in MOFs based on different bis(pyrazolyl)-tagged ligands ([M(BPZ)]n where M = Zn(II), Cu(II), H2BPZ = 4,4′-bipyrazole, [M(BPZ-NH2)]n where M = Zn(II), Cu(II); H2BPZ-NH2 = 3-amino-4,4′-bipyrazole, and [Mx(Me4BPZPh)] where M = Zn(II), x = 1; Cu(II), x = 2; H2Me4BPZPh = bis-4′-(3′,5′-dimethyl)-pyrazolylbenzene) and, for the first time, a detailed study of their antibacterial activity, tested against Gram-negative (E. coli) and Gram-positive (S. aureus) bacteria, as representative agents of infections. The results show that all MOFs exert a broad-spectrum activity and strong efficiency in bacterial growth inhibition, with a mechanism of action based on the surface contact of MOF particles with bacterial cells through the so-called “chelation effect” and reactive oxygen species (ROS) generation, without a significant release of Zn(II) and Cu(II) ions. In addition, morphological changes were elucidated by using a scanning electron microscope (SEM) and bacterial cell damage was further confirmed by a confocal laser scanning microscopy (CLSM) test.